The present project will be directed toward the solution to the following problems relating to MDF and circulatory shock: (1) To determine which proteases and upon what type of substrate they act to catalyze the formation of MDF; (2) To determine the amino acid composition and sequence of MDF. (3) To determine the role of lysosomal proteases in the formation of MDF, and to ascertain the direct effects of lysosomes on the pathogenesis of circulatory shock; (4) To determine the biological fate of MDF in the intact organism, primarily its routes of inactivation or excretion; (5) To determine the biological effects of MDF on platelet function, liver and myocardial cell integrity; (6) To determine the cellular mechanisms of the cardiodepressant effect of MDF and its effect on the spread of infarct size in acute myocardial infection; (7) To study pharmacologic agents which are able to counteract the negative inotropic effect of MDF. BIBLIOGRAPHIC REFERENCES: Flynn, J.T., G.A. Bridenbaugh, and A.M. Lefer. Plasma prostaglandin F2 alpha and 15-keto F2 alpha concentrations during splanchnic artery occlusion shock. Proc. Soc. Exptl. Biol. Med. 151:193-197, 1976. Flynn, J.T., G.A. Bridenbaugh, and A.M. Lefer. Release of prostaglandin F2 alpha during splanchnic artery occlusion shock. Am. J. Physiol. 230:684-690, 1976.